Journal Mobile Options
Table of Contents
Vol. 77, No. 2, 2006
Issue release date: May 2006
Section title: Original Paper
Pharmacology 2006;77:63–70
(DOI:10.1159/000092773)

Effects of Schisandrin B Enantiomers on Cellular Glutathione and Menadione Toxicity in AML12 Hepatocytes

Chiu P.Y. · Leung H.Y. · Poon M.K.T. · Mak D.H.F. · Ko K.M.
Department of Biochemistry, Hong Kong University of Science and Technology, Hong Kong, SAR, China

Do you have an account?

Register and profit from personalized services (MyKarger) Login Information

Please create your User ID & Password





Contact Information









I have read the Karger Terms and Conditions and agree.

Register and profit from personalized services (MyKarger) Login Information

Please create your User ID & Password





Contact Information









I have read the Karger Terms and Conditions and agree.

To view the fulltext, please log in

To view the pdf, please log in

Buy

  • FullText & PDF
  • Unlimited re-access via MyKarger (new!)
  • Unrestricted printing, no saving restrictions for personal use
  • Reduced rates with a PPV account
read more

Direct: USD 38.00
Account: USD 26.50

Select

Rent/Cloud

  • Rent for 48h to view
  • Buy Cloud Access for unlimited viewing via different devices
  • Synchronizing in the ReadCube Cloud
  • Printing and saving restrictions apply

Rental: USD 8.50
Cloud: USD 20.00

Select

Subscribe

  • Access to all articles of the subscribed year(s) guaranteed for 5 years
  • Unlimited re-access via Subscriber Login or MyKarger
  • Unrestricted printing, no saving restrictions for personal use
read more

Subcription rates


Select


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: 1/23/2006
Accepted: 3/9/2006
Published online: 6/2/2006
Issue release date: May 2006

Number of Print Pages: 8
Number of Figures: 5
Number of Tables: 0

ISSN: 0031-7012 (Print)
eISSN: 1423-0313 (Online)

For additional information: http://www.karger.com/PHA

Abstract

Effects of schisandrin B enantiomer ((+)Sch B and (–)Sch B) treatment on the reduced cellular glutathione (GSH) level and susceptibility to menadione-induced toxicity were investigated and compared in AML12 hepatocytes. (+)Sch B or (–)Sch B treatment at 6.25 µmol/l produced a time-dependent change in cellular GSH level, with the maximal stimulation occurring 16 h after dosing. (+)Sch B/(–)Sch B pretreatment for 16 h dose-dependently protected against menadione toxicity, with the maximum degree of protection observable at 6.25 µmol/l and the extent of protection afforded by (–)Sch B being larger than that of (+)Sch B. The cytoprotection was associated with a parallel enhancement in cellular GSH level in both non-menadione (control) and menadione-intoxicated cells. While the GSH depletion produced by buthionine sulfoximine/phorone treatment largely abrogated the cytoprotective action of (+)Sch B/(–)Sch B, it almost completely abolished the GSH-enhancing effect of (+)Sch B and (–)Sch B in both control and menadione-treated cells. Both (+)Sch B and (–)Sch B treatments increased the GSH reductase activity in control and menadione-treated cells, with the stimulatory action of (–)Sch B being more potent than that of (+)Sch B in the control condition. (+)Sch B and (–)Sch B also enhanced the γ-glutamate cysteine ligase activity in menadione-intoxicated cells. The results indicate that (–)Sch B is more effective than (+)Sch B in enhancing cellular GSH and protecting against oxidant injury in hepatocytes.

© 2006 S. Karger AG, Basel


  

Author Contacts

Kam Ming Ko
Department of Biochemistry
Hong Kong University of Science and Technology
Clear Water Bay, Hong Kong, SAR (China)
Tel. +852 2358 7298, Fax +852 2358 1552, E-Mail bcrko@ust.hk

  

Article Information

Received: January 23, 2006
Accepted: March 9, 2006
Published online: April 21, 2006
Number of Print Pages : 8
Number of Figures : 5, Number of Tables : 0, Number of References : 26

  

Publication Details

Pharmacology (International Journal of Experimental and Clinical Pharmacology)

Vol. 77, No. 2, Year 2006 (Cover Date: May 2006)

Journal Editor: Donnerer, J. (Graz)
ISSN: 0031–7012 (print), 1423–0313 (Online)

For additional information: http://www.karger.com/PHA


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: 1/23/2006
Accepted: 3/9/2006
Published online: 6/2/2006
Issue release date: May 2006

Number of Print Pages: 8
Number of Figures: 5
Number of Tables: 0

ISSN: 0031-7012 (Print)
eISSN: 1423-0313 (Online)

For additional information: http://www.karger.com/PHA


Copyright / Drug Dosage

Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher or, in the case of photocopying, direct payment of a specified fee to the Copyright Clearance Center.
Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in goverment regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.